A CREB1/miR-433 reciprocal feedback loop modulates proliferation and metastasis in colorectal cancer

Li, Yan; You, Weiqiang; Sheng, Nengquan; Gong, Jianfeng; Hu, Landian; Tan, Gewen; Chen, Hongqi; Wang, Zhigang

doi:10.18632/aging.101671

Cited by 38 publications

(31 citation statements)

References 43 publications

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“…17 As for in GC, an inhibitor of CREB1, miR-1297, was found to be poorly existed in GC patients and positively correlated with survival of patients. 18 Promotion of CREB1 in cancer has also been evidenced in several tumor cell types involving bladder cancer, 19 colorectal cancer 20 and glioma 21 cells. Likewise, high-expression profiles of CREB1 have also been found in GC cell lines and its downregulation led to declines in growth and migration of SGC-7901 cells.…”

Section: Discussionmentioning

confidence: 97%

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

Huang

Liu

Jiang

et al. 2020

CMAR

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Background: The cAMP response element-binding protein 1 (CREB1) was initiated as a potential target for cancer treatment. This research was conducted to probe the effect of CREB1 in the progression of gastric cancer (GC) and the molecules involved. Materials and Methods: CREB1 expression in GC tissues and cell lines (AGS and MKN-45) as well as that in normal tissues and in gastric mucosa cell line (GES-1) was detected. The correlation between CREB1 expression and prognosis of GC patients was determined. Artificial silencing of CREB1 was introduced to evaluate its effect on biological behaviors of GC cells. The target microRNA (miRNA) of CREB1 and the target mRNA of miR-186 were predicted and validated. Altered expression of miR-186, KRT8 and HIF-1α was introduced to confirm their functions in GC progression. Results: CREB1 was abundantly expressed in GC tissues and cells and linked to dismal prognosis in patients. Silencing of CREB1 or upregulation of miR-186 suppressed the malignant behaviors such as growth, epithelial-mesenchymal transition (EMT) and invasion of GC cells, while artificial overexpression of KRT8 led to reversed trends. KRT8 was a target mRNA of miR-186, and CREB1 transcriptionally suppressed miR-186 expression to further up-regulate KRT8. KRT8 was also found to increase HIF-1α expression. Upregulation of HIF-1α was found to block the suppressing role of CREB1 silencing in GC cell malignancy. Conclusion: This study evidenced that silencing of CREB1 inhibits growth, invasion, EMT and resistance to apoptosis of GC cells involving the upregulation of miR-186 and the following downregulation of KRT8 and HIF-1α.

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Section: Discussionmentioning

confidence: 97%

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

Huang

Liu

Jiang

et al. 2020

CMAR

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“…Several miRNAs, such as miR-134-5p, miR-27a-5p, and miR-342-3p, target the PKG downstream molecule Creb1; novel_circ_000915 can also target Creb1 and function as a ceRNA pair according to our prediction. In colon cancer, miR-433 inhibits Creb1 and exerts an antitumor effect by inhibiting the cell cycle [ 27 ]. Creb1 is also a direct target of miR-122, which can promote cell proliferation and invasion in bladder cancer [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

RNA interactions in right ventricular dysfunction induced type II cardiorenal syndrome

Chen

Huang

Xie

et al. 2021

Aging

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Right ventricular (RV) dysfunction induced type II cardiorenal syndrome (CRS) has a high mortality rate, but little attention has been paid to this disease, and its unique molecular characteristics remain unclear. This study aims to investigate the transcriptomic expression profile in this disease and identify key RNA pairs that regulate related molecular signaling networks. We established an RV dysfunction-induced type II CRS mouse model by pulmonary artery constriction (PAC). PAC mice developed severe RV hypertrophy and fibrosis; renal atrophy and dysfunction with elevated creatinine were subsequently observed. Expression profiles in RV and kidney tissues were obtained by whole transcriptome sequencing, revealing a total of 741 and 86 differentially expressed (DE) mRNAs, 159 and 29 DEmiRNAs and 233 and 104 DEcircRNAs between RV and kidney tissue, respectively. Competing endogenous RNA (ceRNA) networks were established. A significant alteration in proliferative, fibrotic and metabolic pathways was found based on GO and KEGG analyses, and the network revealed key ceRNA pairs, such as novel_circ_002631/miR-181a-5p/Creb1 and novel_circ_002631/miR-33-y/Kpan6. These findings indicate that significantly dysregulated pathways in RV dysfunction induced type II CRS include Ras, PI3K/Akt, cGMP-PKG pathways, and thyroid metabolic pathways. These ceRNA pairs can be considered potential targets for the treatment of type II CRS.

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“… 37 , 38 In our study, we identified that CREB1 was upregulated in CRC tissues and cells, and the similar results upon CREB1 in CRC were documented in the previous study. 39 Interestingly, CREB1 was a target of miR-519d-3p. Moreover, the CREB1 protein expression was upregulated in CRC cells treated with co-transfection of both si-BLACAT1 and anti-miR-519d-3p in comparison with transfection of si-BLACAT1 solely in vitro.…”

Section: Discussionmentioning

confidence: 99%

LncRNA BLACAT1/miR-519d-3p/CREB1 Axis Mediates Proliferation, Apoptosis, Migration, Invasion, and Drug-Resistance in Colorectal Cancer Progression

Chen¹,

Zhou²,

Chen³

et al. 2020

CMAR

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Background Colorectal cancer (CRC) is a common severe disease around the world. The merging papers reported that long noncoding RNAs (lncRNAs) took part in the diversified pathological processes of CRC. This study aimed to uncover the role and the potential mechanism of lncRNA bladder cancer-associated transcript 1 (BLACAT1) in CRC progression. Methods LncRNA BLACAT1, micro-519d-3p (miR-519d-3p), and cAMP-responsive element binding protein 1 ( CREB1 ) levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in CRC tissues and cells. The bio-functional effects were examined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry assay, and transwell assay. The susceptibility testing was determined by oxaliplatin (OXA) administration. The potential binding sites between miR-519d-3p and BLACAT1 or CREB1 were predicted by online software starBase and confirmed by dual-luciferase reporter analysis. The relative proteins expression in CRC cells was determined by Western blot analysis. Xenograft tumor model was used to evaluate biological function of BLACAT1 in vivo. Results The expression of BLACAT1 was promoted in CRC tissues and cells, and correlated to the TNM (tumor, node, metastasis) stage, distant metastasis, and overall survival rate. Silencing of BLACAT1 limited the proliferation, migration, and invasion, facilitated the apoptosis, and re-sensitized OXA-resistance in CRC cells. MiR-519d-3p was a target of BLACAT1. Furthermore, miR-519d-3p deletion reversed the positive effects of BLACAT1 deletion on CRC cells. Moreover, our data showed that miR-519d-3p directly targeted CREB1 and BLACAT1 sponged miR-519d-3p to regulate CREB1 expression. Besides, CREB1 disrupted the bio-functional results above from BLACAT1 suppression. Additionally, BLACAT1 knockdown promoted CRC cells sensitivity to OXA in vivo. Conclusion BLACAT1 mediated the progression of CRC and OXA-resistance by miR-519d-3p/ CREB1 axis.

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A CREB1/miR-433 reciprocal feedback loop modulates proliferation and metastasis in colorectal cancer

Cited by 38 publications

References 43 publications

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

<p>CREB1 Suppresses Transcription of microRNA-186 to Promote Growth, Invasion and Epithelial–Mesenchymal Transition of Gastric Cancer Cells Through the KRT8/HIF-1α Axis</p>

RNA interactions in right ventricular dysfunction induced type II cardiorenal syndrome

LncRNA BLACAT1/miR-519d-3p/CREB1 Axis Mediates Proliferation, Apoptosis, Migration, Invasion, and Drug-Resistance in Colorectal Cancer Progression

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